Ankrd17 positively regulates RIG-I-like receptor (RLR)-mediated immune signaling.

Retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), such as RIG-I, melanoma differentiation-associated gene 5 (MDA5), and virus-induced signaling adaptor (VISA), are intracellular molecules that sense diverse viral RNAs and trigger immune responses. In this study, we demonstrate that the ankyrin repeat protein ankrd17 interacts with RIG-I, MDA5, and VISA and upregulates RLR-mediated immune signaling. Overexpression of ankrd17 enhances RLR-mediated activation of IRF-3 and NF-κB and upregulates the transcription of IFN-β. It also promotes RLR signaling in response to poly (I:C), influenza virus RNA, and Sendai virus. Consistently, knockdown of ankrd17 impairs RLR signaling. Furthermore, we demonstrate that ankrd17 enhances the interaction of RIG-I and MDA5 with VISA; the ankyrin repeat domain of ankrd17 is required for its interaction with RIG-I as well as for its function in regulating the RLR pathway. Taken together, our results indicate that ankrd17 is a positive regulator of the RLR signaling pathway.

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